Obesity Diabetes And Inflammation

Obesity is a worldwide epidemic that affects half a billion people. It has been estimated that, if current trends continue, by 2050, 60% of men and 50% of women worldwide will be obese. Hypertrophy and hyperplasia of white adipose tissue caused by overweight and obesity lead to a chronic inflammatory state, which results in impaired insulin sensitivity and the development of diabetes. Currently, the number of people affected by diabetes globally exceeds 400 million (rising more rapidly in low- and middle-income countries). In 2019, diabetes was the ninth leading cause of mortality, with an estimated 1.5 million direct deaths. This book provides a comprehensive overview of the relationship between inflammation, obesity, and diabetes. It focuses on the pathogenesis and biological mechanisms of obesity, the interaction between adipose tissue and the immune system, the role of genetic and environmental factors, the progression of cardiovascular complications, and the association of obesity and inflammation with type 1 and type 2 diabetes, as well as gestational diabetes. This volume also includes practical recommendations for preventing and managing these conditions using both lifestyle modifications and pharmacological interventions. Written by experts in the field, Obesity, Diabetes and Inflammation: Molecular Mechanisms and Clinical Management addresses the role of inflammation in both obesity and diabetes, its effect on vascular and non-vascular pathologies, oxidative stress, genetics, and epigenetics. This text aims to be a valuable resource for researchers, clinicians, and students of medicine at all levels.

Characterized by obesity, insulin resistance, dyslipidemia, and hypertension, metabolic syndrome is associated with the risks of type 2 diabetes mellitus and cardiovascular disease. Obesity, which increases the incidence of atherosclerotic cardiovascular disease and subsequently leads to increased stress and inflammation, appears to play a central role in the progression of the syndrome. Evidence of inflammatory processes in accumulated fat appears to be an early initiator of metabolic syndrome. Likewise, the more active angiotensin system in obesity may contribute to even greater oxidative stress that serves as a key signaling event in vascular remodeling. These factors strengthen obesity's association with oxidative stress. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome is designed to encourage the development of evidence-based nutritional and pharmacological therapies that can attenuate the impact of obesity-induced insulin resistance and ensuing metabolic syndrome. The book offers a deep understanding of the molecular mechanisms that underlie the process. Edited by leading authorities on oxidative stress, the book's chapters report on cutting-edge research that explores intracellular events mediating or preventing oxidative stress and pro-inflammatory processes in obesity and type 2 diabetes. It also brings together research on the molecular mechanisms inherent in the progression of metabolic stress, includes phenotypic perspectives, and discusses dietary factors, including the role of micronutrients. The chapter authors, each a leading expert in his or her field, discuss different components of metabolic stress and obesity and their associations with oxidative stress and inflammation. The book fills a unique role as a base of knowledge for researchers seeking to develop nutritional and or pharmacological therapies, as well as clinicians seeking a better understanding of this increasingly common disease process.

For decades, scientific efforts have been made to understand obesity and related diseases such as type 2 diabetes and neurodegeneration, and their link with meta-inflammation. Adipose tissue is, at present, viewed as an endocrine organ with important biological effects on metabolism and inflammation, with a possible role in the pathogenesis of obesity-associated metabolic and inflammatory diseases. Chronic systemic low-grade inflammation has gained significant attention as the key player in the pathophysiology of obesity- and aging-associated diseases. Keeping view of this trend, Meta-Inflammation and Obesity offers readers state-of-the-art knowledge on this subject. Chapters cover special topics such as gender differences in obesity-related type 2 diabetes as the consequence of inflammatory response, insights into metabolic changes caused by excessive adipose tissue (which lead to abnormal brain metabolism, neuroinflammation, cognitive decline, development of type 3 diabetes), and the importance of inflammaging in the aging process. Graduate, postgraduate and Ph. D. candidates in medicine, pharmacy, and students of applied medicine, health care professionals as well as scientists involved in adipose tissue research, meta-inflammation analysis, obesity-related medical specialties will find this book a useful reference on the link between inflammation and obesity.

Immune response and metabolic regulation are highly integrated and this interface maintains a central homeostatic system, dysfunction of which can cause obesity-associated metabolic disorder such as type 2 diabetes, fatty liver disease and cardiovascular disease. Insulin resistance is an underlying basis for the pathogenesis of these metabolic diseases. Overnutrition or obesity activates the innate immune system with subsequent recruitment of immune cells such as macrophages and T cells, which contributes to the development of insulin resistance. In particular, a significant advance in our understanding of obesity-associated inflammation and insulin resistance has been recognition of the critical role of adipose tissue macrophages (ATMs). ATMs are a prominent source of proinflammatory cytokines, such as TNF-a and IL-6, that can block insulin action in adipose tissue, skeletal muscle, and liver autocrine/paracrine signaling and cause systemic insulin resistance via endocrine signaling, providing a potential link between inflammation and insulin resistance. All articles in this topic highlight the interconnection between obesity, inflammation, and insulin resistance in all its diversity to the mechanisms of obesity-induced inflammation and role of immune system in the pathogenesis of insulin resistance and diabetes.

The American Obesity Association identifies obesity's link to numerous medical conditions, including hypertension, type 2 diabetes, cardiovascular disease, several cancers, and a host of inflammatory disorders. Evidence indicates that inflammation has more than a corollary relation with obesity; that in fact, obesity itself manifests a low-grade, m

In addition to its metabolic and endocrinologic effects, obesity and adipose tissue have now been shown to be associated with low grade inflammation resulting in cellular and humoral inflammatory factors of which the latter may act by endocrine, paracrine and autocrine mechanisms. These inflammatory mediators have increasingly been suggested as contributing to the obesity link to carcinogenesis and cancer promotion. This volume of Energy Balance and Cancer will focus on recent developments and cutting edge research pointing to inflammation and inflammatory factors as key mediators of this linkage. The volume first provides information on inflammation as an important link between obesity and insulin resistance, which is in itself linked to promotion of cancer through hyperinsulinemia. The volume then covers some of the most important mechanisms by which obesity leads to inflammation, including the novel inflammasome concept, alterations in chromatin structure, circulating inflammatory factors, unique cellular interactions between adipocytes and macrophages and the direct link of dietary fat to inflammation and cancer. Overall, this volume will provide important insight to help understand how inflammation may help modulate the linkage between obesity and cancer and serve as a platform for developing future research in this area.

​According to the World Health Organization, the epidemic of global obesity has nearly tripled since 1975. In 2016, more than 1.9 billion adults were overweight, over 650 million of which were obese. Being overweight and obese has been linked to a number of non-communicable, chronic diseases. Pathophysiology of Obesity-Induced Health Complications is a compilation of review articles dedicated to describe co-morbidities associated with obesity. The wide range that is covered is of significant interest to basic research scientists, clinicians and graduate students who are engaged in studying obesity-induced health complications. Furthermore, this book highlights the potential of novel approaches for the prevention and treatment of obesity and its related illnesses. Nineteen articles in this book are organized in four sections that are designed to provide an overview of obesity-induced health complications. The first section serves as an introductory section on the prevalence, causes, consequences, treatments and preventive approaches for obesity. Section two covers the metabolic disturbances and inflammation due to obesity. The third section is focused on neurological and visceral complications as a consequence of obesity. The final section covers strategies for the prevention of obesity-induced complications. The book illustrates that obesity can result in a diverse range of pathophysiological conditions that adversely affect health.